Interaction of triphenyltin and an agonist of retinoid X receptor (LGD1069) in embryos of Xenopus tropicalis

Xenopus tropicalis embryos were exposed for 48 h to mixtures of triphenyltin and LGD1069 (an agonist of the retinoid X receptor). The index of fin deficiency (IFD) of the embryos increased in the triphenyltin-treated groups, and the index of axis deficiency (IAD) increased in LGD1069-treated groups in a concentration-dependent manner. When embryos were exposed to mixtures of 5 μg Sn/L triphenyltin and 1-30 μg/L LGD1069, IFD decreased from 2.9 to 0.6 and IAD increased from 0.1 to 2.4 with increasing LGD1069 concentrations. Conversely, when embryos were exposed to mixtures of 15 μg/L LGD1069 and 1-10 μg Sn/L triphenyltin, IFD increased from 0.1 to 3.0 with increasing triphenyltin concentrations. Co-exposure induced some new phenotypes, such as posteriorized anus. These results suggest that LGD1069 suppressed the teratogenicity of triphenyltin and that the retinoid X receptor was involved in triphenyltin-induced teratogenicity. Histological observations indicate that co-exposure inhibited the invagination of the yolk plug.

► Triphenyltin induces enlarged proctodaeums and narrow fins in frog embryos. ► LGD1069 suppressed the teratogenic effects of triphenyltin. ► Triphenyltin did not affect the teratogenic effects of LGD1069. ► Combined exposure to triphenyltin and LGD1069 induced more variable malformations. ► The retinoid X receptor was involved in triphenyltin-induced teratogenicity.